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Review
. 2020 Oct 1;147(7):1793-1807.
doi: 10.1002/ijc.32987. Epub 2020 Apr 21.

Caveolin-1 in oncogenic metabolic symbiosis

Martina Raudenska  1 , Jaromir Gumulec  1   2   3 , Jan Balvan  1   2   3 , Michal Masarik  1   2   4
Affiliations
Review

Caveolin-1 in oncogenic metabolic symbiosis

Martina Raudenska et al. Int J Cancer. .

Abstract

Metabolic phenotypes of cancer cells are heterogeneous and flexible as a tumor mass is a hurriedly evolving system capable of constant adaptation to oxygen and nutrient availability. The exact type of cancer metabolism arises from the combined effects of factors intrinsic to the cancer cells and factors proposed by the tumor microenvironment. As a result, a condition termed oncogenic metabolic symbiosis in which components of the tumor microenvironment (TME) promote tumor growth often occurs. Understanding how oncogenic metabolic symbiosis emerges and evolves is crucial for perceiving tumorigenesis. The process by which tumor cells reprogram their TME involves many mechanisms, including changes in intercellular communication, alterations in metabolic phenotypes of TME cells, and rearrangement of the extracellular matrix. It is possible that one molecule with a pleiotropic effect such as Caveolin-1 may affect many of these pathways. Here, we discuss the significance of Caveolin-1 in establishing metabolic symbiosis in TME.

Keywords: Caveolin-1; cancer; cancer-associated fibroblast; glycolysis; metabolic symbiosis; metabolism; tumor microenvironment.

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References

    1. Pavlova NN, Thompson CB. The emerging hallmarks of cancer metabolism. Cell Metab 2016;23:27-47.
    1. Lyssiotis CA, Kimmelman AC. Metabolic interactions in the tumor microenvironment. Trends Cell Biol 2017;27:863-75.
    1. Mangia S, Simpson IA, Vannucci SJ, et al. The in vivo neuron-to-astrocyte lactate shuttle in human brain: evidence from modeling of measured lactate levels during visual stimulation. J Neurochem 2009;109:55-62.
    1. Nishiyama K, Trapp BD, Ikezu T, et al. Caveolin-3 upregulation activates beta-secretase-mediated cleavage of the amyloid precursor protein in Alzheimer's disease. J Neurosci 1999;19:6538-48.
    1. Song KS, Scherer PE, Tang Z, et al. Expression of caveolin-3 in skeletal, cardiac, and smooth muscle cells. Caveolin-3 is a component of the sarcolemma and co-fractionates with dystrophin and dystrophin-associated glycoproteins. J Biol Chem 1996;271:15160-5.

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